Information about the external temperature is provided by thermoreceptors in the skin. Core body temperature is monitored by central thermoreceptive neurons in the preoptic area (and possibly the spinal cord), which monitor the temperature of local blood. Thermoreceptors in the viscera monitor the temperature in these organs. All of these receptors provide temperature information to the preoptic area (pathways described later), along with parts of the hypothalamus, in which this information is used to keep core body temperature constant. Thus the preoptic area and hypothalamus act together as a servomechanism with a set point at the normal body temperature.
Although the signals from each of these sources are integrated, their relative importance may shift, depending on the situation. Changes in environmental temperature evoke more rapid and much larger changes in the temperature of the skin than in the body core, and so cutaneous receptors are probably the initial and most often used mechanism for compensating for external changes in temperature. Central thermoreceptors are more important for situations with internal causes of temperature change, such as during exercise, or in which external changes temperature are so severe or prolonged that core body temperature starts to change despite the signals from peripheral thermoreceptors. Last, alteration of body temperature by ingestion of hot or cold food or liquids is detected by the visceral thermoreceptors.
Error signals (i.e., cooling and warming of the body), which represent a deviation from the set point of the servomechanism, evoke responses that tend to restore body temperature toward the set point. These responses are mediated by the autonomic, somatic, and endocrine systems.
Situations involving cooling, for example, trigger a variety of responses that increase heat production (thermogenesis) and minimize heat loss. Heat production is increased by mechanisms that include shivering thermogenesis (asynchronous contractions of skeletal muscle that increases heat production) and brown adipose tissue (BAT) thermogenesis (in BAT thermogenesis, oxidative phosphorylation is uncoupled from ATP synthesis, which allows the energy released by the reaction to be dissipated as heat instead), and increased thyroid hormone levels lead to increased metabolism. Heat loss is reduced by cutaneous vasoconstriction and by piloerection. Piloerection is effective in animals with fur but not in humans; in the latter, the result is only goose bumps. In addition, tachycardia occurs, which may help provide metabolites to be used in thermogenesis to the thermogenic tissues (fat and muscle) and help distribute the heat generated throughout the body. Finally, the perception of being cold influences the decision to initiate voluntary behaviors: in this case, possibly putting on a jacket.
Warming the body generally causes changes in the opposite direction. The activity of the thyroid gland diminishes, which leads to reduced metabolic activity and less heat production. Heat loss is increased by sweating, salivation (in some animals but not humans), and cutaneous vasodilation (because of decreased sympathetic activity). However, again tachycardia occurs, this time presumably to allow optimal perfusion of the cutaneous circulation for heat dissipation.
Early studies identified the preoptic region and anterior hypothalamus as a heat loss center and the posterior hypothalamus as a heat conservation center. For example, lesions in the preoptic region prevent sweating and cutaneous vasodilation, and if an individual with a lesion in this region is placed in a warm environment, hyperthermia occurs. Conversely, electrical stimulation of the heat loss center causes cutaneous vasodilation and inhibits shivering. In contrast, lesions in the area dorsolateral to the mammillary body interfere with heat production and conservation and can cause hypothermia when the person is in a cold environment. Electrical stimulation in this region of the brain evokes shivering.